Below, is the official statement that we have received from Professors Greg Towers and Paul Kellam:

On 20 December 2010, the peer-review journal Retrovirology published a series of papers relating to XMRV, a virus previously linked to CFS/ME. These included our paper, Disease-associated XMRV sequences are consistent with laboratory contamination by Hue et al at University College London (UCL) and the Wellcome Trust Sanger Institute, with funding from a number of organisations including the Wellcome Trust.

In our study, we showed that it is extremely unlikely that XMRV is a human pathogen or one which transmits between humans. There has been much discussion of what exactly we can and did conclude from our observations. We would like to take this opportunity to reiterate the following.

Comparison of XMRV found in patients and XMRV found in the prostate cancer cell line 22Rv1 tells us that patient-derived XMRV sequences do not contain sequence variation that invariably accompanies transmission of retroviruses between individuals. XMRV is like any other virus: it has a genome, which, when replicated during the process of infection, accumulates mutations, with the number of mutations acting as a counter for the number of replication events. XMRV is not able to replicate without variation and we showed this by determining the sequence variation of the virus in the 22Rv1 cells. Thus we can conclude that XMRV sequences from CFS samples are not from a virus that has transmitted between individuals and thus cannot be the cause of chronic fatigue syndrome or prostate cancer.

The Scicasts blog contains some criticism of our methodology and the fact that we addressed only one component of the research originally published in Science. We used established scientifically accepted and rigorous protocols that are in no way dependent on user bias. We, and the other papers in Retrovirology, did indeed address one component of the research originally published in Science, namely that of PCR assays. However, this type of assay is used in all XMRV and CFS studies, is the most sensitive and when coupled with sequence analysis the most specific. Therefore by showing that the original assertions that are made using this assay are flawed we conclude that those studies are compromised.

Our study did not address the issue of anti-MLV antibodies in CFS patients and we therefore cannot conclude anything about these observations. However, we would expect to see the description of anti-MLV antibodies in CFS patients to be reported in more than one laboratory before this technique was used diagnostically. To the best of our knowledge, no other peer-reviewed research has been able to provide evidence of anti-MLV antibodies in CFS patients.

We recognise that chronic fatigue syndrome/ME is a very real and distressing condition. It is important to recognize that we are not claiming that CFS/ME is not caused by a virus this may well still be the case. It is still not clear what causes the condition and it is important that scientists explore all avenues of research to identify its cause or causes and enable better treatments.

We are committed to understanding and identifying virus causes of human disease. We are similarly committed to giving both the scientific community and lay audiences accounts of the findings of their work, and that was what motivated us to issue our joint press release.

"Thus we can conclude that XMRV sequences from CFS samples are not from a virus that has transmitted between individuals and thus cannot be the cause of chronic fatigue syndrome or prostate cancer."

They just can't help themselves with the logical non-sequitors, can they? Even if one accepts the premise, the conclusion just doesn't follow at all. It just boggles the mind how such illogical reasoning gets to be taken seriously.

As John Coffin explained at the blood working group, these same observations could be explained by the well-known mechanism of a series of local outbreaks originating in each case from a single mouse.

As the Dutch paper explained, the lack of sequence variability could also be explained by vaccine-medicated transmission, which is theoretically entirely possible and has not previously been screened for - the Hue et al findings just make that possibility more likely.

So quite apart from the other problems with Hue et al's analysis (their statistical assumptions, the small number of sequences they're based on, the fact they aren't relevant to Hanson's, Lo's and Alter's work, etc), the conclusions they draw from that analysis just aren't valid at all - they quite obviously don't follow logically.

And when did we go from "this doesn't make sense because CFS doesn't seem to be virally transmitted from individual" to "this can't be the cause of CFS because it looks like it hasn't been transmitted from individual to individual"? These Catch-22s come so thick and fast these days, it's hard to keep up with the latest spurious justification for doing nothing at all.

Our study did not address the issue of anti-MLV antibodies in CFS patients and we therefore cannot conclude anything about these observations. However, we would expect to see the description of anti-MLV antibodies in CFS patients to be reported in more than one laboratory before this technique was used diagnostically. To the best of our knowledge, no other peer-reviewed research has been able to provide evidence of anti-MLV antibodies in CFS patients.

erm Didnt doctor Sing report recently that she detected a specific xmrv anti body response in a ME/CFS patient ? if so, then the xmrv anti body from just one lab argument wouldnt seem to hold up, just a thought

erm Didnt doctor Sing report recently that she detected a specific xmrv anti body response in a ME/CFS patient ? if so, then the xmrv anti body from just one lab argument wouldnt seem to hold up, just a thought

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I am with you here, but I don't think Singh has published about this. And so it's not official.

It hasn't been published yet, but Bagni is also finding antibody differences between WPI-provided positives and healthy controls. Whether Singh, Bagni, or anybody else, will ever be allowed to publish those findings, I guess we will find out this year...

To the best of our knowledge, no other peer-reviewed research has been able to provide evidence of anti-MLV antibodies in CFS patients.

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I suspect that there are papers that prove this, but they have been waiting, waiting and waiting to be published. There are quite a few papers waiting to be published and it ills me to no end as these papers I feel sure would squelch this contamination theory. As well, they would probably accelerate various treatments to give us some relief from this disease. I understand researchers have to make a living, but if there is information that would provide help for our pain then it needs to be known to us without taking a year to get published!

Their first argument is the "lack of variation", but hasn't this claim been debunked already, albeit with unpublished data from several different researchers?

Their second argument is about the PCR assays but they did not respond to the points raised by the criticism, merely stated that they are right:

The Scicasts blog contains some criticism [from its readers] of our methodology and the fact that we addressed only one component of the research originally published in Science. We used established scientifically accepted and rigorous protocols that are in no way dependent on user bias. We, and the other papers in Retrovirology, did indeed address one component of the research originally published in Science, namely that of PCR assays. However, this type of assay is used in all XMRV and CFS studies, is the most sensitive and when coupled with sequence analysis the most specific. Therefore by showing that the original assertions that are made using this assay are flawed we conclude that those studies are compromised.

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<sarcasm>Gee, what a comeback.</sarcasm>

I guess pMLV's are included in their stance, or is the Lo/Alter paper the elephant in the room? It will be interesting to see a professional rebuttal from researchers who believe HGRV is relevant.

No substantive response to the issues raised and of course no acknowledgment that their press release wildly exaggerated what the Hue paper claimed to demonstrate. I do find two points slightly interesting: this time around, they clarified that oh yes, they ARE also claiming the previous prostate cancer research was all wrong too (having barely mentioned prostate cancer in their original release); and that they are so insistent on reiterating that ME/CFS *might* still have a viral cause, just not this one. One wonders if they've got another candidate in mind, and if so, what??

I am with you here, but I don't think Singh has published about this. And so it's not official.

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True Jemal, but the fact that she has, really argues against there assumptions. And if they want to concentrate on published as being more important than the science information itself, then clearly they are using situations against us, to bolster there veiw point. when really in reality its as weak as saying, well its not published so not realiable lol. who are they kidding they really think Dr sing is wrong about this, her science is flawed because its not published yet. They are splitting hairs now, and ignoring the science by doing so.Yesterdays reports are tommorows published evidence. They are clearly stalling for time playing this game, and there time will be running out when said such data is published. But of course by playing the game the way wessley would, really makes it harder ( or even less likely ) that such said data will get published or see the light of day. Thats what this is really all about making those kind of statements, its a clever little stalling tactic, trying to put a spanner in the works, and hope it does enough damage that such said evidence never sees the light of day. Vey clever. very clever way of trying to shut us up

Hi, I posted this on another thread but perhaps it belongs here. I was thinking that since some of us have CFS for decades and do not get worse or die but instead may have remissions perhaps an infectious agent with very low replication is to be expected? I would assume that a rapidly multiplying virus would overcome the body's defences and kill its host or at least cause obvious damage. (not the subtle damage we see in CFS, which leads to questioning whether we are ill at all)
Perhaps low replication is to be expected? and not an argument against XMRV?

Dr Miller said on another forum that it was harder for him to get funding to study XMRV due to the contamination claims. So their "stalling" tactics have a real effect on the science.

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Theres the proof its working right there, thanks for pointing that out, What we really need to see is a anti body test that can be proven to be 100% specific to xmrv, then we really will know infection is really happening. But thats as far as the nay sayers are concernerd. I belive that infection is happienng. The monkey studies really seem to suggest strongly thats likely, as does other evidence. I wonder if this 100% specific anti body test will be published at any point and who that will come from. Just out of interest does the the wpi consider there anti body testing to be specific. and if so anyone know to what level of certainty they feel it is, these are very important questions relating to the hue paper. we really do need to go beyond this squabbling, and prove once and for all its in the patients, and then look for what it could actually be doing, in my case im starting to belive it can create intermitent auto immunity. as ive shown some of those symptoms, but they appear to be able to come and go, or worsen and improve.